Lung diseases include many known inflammatory lung diseases such as acute bronchitis due to acute inflammation caused by viruses, bacteria, or the like; chronic bronchial asthma mainly developed from respiratory tract inflammation due to eosinophils; interstitial pneumonia involving lung structure damage caused by alveolar epithelial inflammation; and chronic obstructive pulmonary disease (COPD), which is known as a disease characterized by chronic pulmonary inflammation caused by various factors, especially smoking, leading to alveolar wall destruction and bronchial mucous gland hypertrophy and the like resulting in shortness of breath, increased cough and sputum, etc.
In the pathological process of the inflammatory lung diseases as described above, it has been known that transmitters, called chemotactic factors, released at early stage will stimulate inflammatory cells, such as neutrophils, basophils, eosinophils, and macrophages and the like, to migrate to local sites and the migrated inflammatory cells will release injurious enzymes and radicals to damage tissues and at the same time will release cytokine or the like, resulting in further migration and activation of the inflammatory cells. When such inflammation develops in respiratory tracts, the infiltrating inflammatory cells will damage bronchial and pulmonary tissues. This finally leads to impairment of respiratory function, including reduction in respiratory flow and oxygen exchange capacity, characteristic of each of the diseases. Lung structure and function are further markedly suppressed, and many cases may progress to intractable diseases that will eventually lead to fibrogenesis or honeycomb lung.
Such inflammatory lung diseases have been treated with drugs with anti-inflammatory effects, and mild to moderate bronchial asthma has been known to completely response to adrenocortical steroids (see Non Patent Literature 1). Interstitial pneumonia has been also treated with adrenocortical steroids at acute exacerbation and combined with immunosuppressive agents where appropriate. Further progression will certainly induce hypoxemia and therefore require oxygen therapy including home oxygen therapy. Adrenocortical steroids have been reported to prevent exacerbation of COPD but their effects on the pathology of COPD are limited (see Non Patent Literature 2). Pulmonary fibrosis has been also treated with steroid therapy although lesions often remain and acute exacerbations are frequently observed due to side effects or reduction or withdrawal of steroidal agents. This is never satisfying in clinical cure and therefore there are needs to develop novel therapeutic agents.
AT Rich Interactive Domain 5A (hereinafter abbreviated as Arid5A) has been reported to be a protein that stabilizes IL-6 mRNA (see, e.g., Non Patent Literature 3).